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Influence of percutaneous coronary intervention on coronary microvascular resistance index
Bart-Jan Verhoeff1, Maria Siebes, Martijn Meuwissen
1Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Insights
Percutaneous coronary interventions (PCI) reduce hyperemic microvascular resistance (h-MR(v)) by restoring distal pressure. This suggests microvascular remodeling may occur after long-term low-pressure exposure.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Physiology
Background:
- Coronary microvascular resistance (h-MR(v)) is typically assumed unchanged post-PCI.
- A novel dual-sensor guidewire assessed h-MR(v) before and after PCI.
Purpose of the Study:
- To test the hypothesis that PCI affects coronary microvascular resistance.
- To evaluate the velocity-based index of hyperemic microvascular resistance (h-MR(v)) post-PCI.
Main Methods:
- Simultaneous measurement of distal coronary pressure and flow velocity during maximal hyperemia (adenosine).
- Measurements taken in reference and target vessels before and after PCI, including stenting.
- Utilized a novel Doppler velocity and pressure-equipped guidewire.
Main Results:
- PCI significantly reduced h-MR(v) (from 2.74 to 1.58 mm Hg·s/cm) and increased distal pressure (from 57.9 to 85.5 mm Hg).
- The reduction in h-MR(v) contributed 34% to the overall decrease in coronary resistance.
- Post-PCI h-MR(v) was lower than the reference vessel's, despite higher reference vessel pressure.
Conclusions:
- PCI-induced pressure restoration reduces h-MR(v), demonstrating pressure dependence.
- Lowered post-PCI and baseline h-MR(v) suggest microvascular remodeling from chronic low-pressure exposure.
Background:
Coronary microvascular resistance during maximal hyperemia is generally assumed to be unaffected by percutaneous coronary interventions (PCIs). We assessed a velocity-based index of hyperemic microvascular resistance (h-MR(v)) by using prototypes of a novel, dual-sensor (Doppler velocity and pressure)-equipped guidewire before and after PCI to test this hypothesis.
Methods And Results:
Aortic pressure, flow velocity (h-v), and pressure (h-P(d)) distal to 24 coronary lesions were measured simultaneously during maximal hyperemia induced by intracoronary adenosine. Measurements were obtained in the reference vessel before PCI and in the target vessel before and after PCI, stenting, and ultrasound-guided, upsized stenting. h-P(d) increased from 57.9+/-17.0 to 85.5+/-15.6 mm Hg, and h-MR(v) (ie, h-P(d)/h-v) decreased from 2.74+/-1.40 to 1.58+/-0.61 mm Hg x cm(-1) . s after stenting (both P<0.001). The reduction in h-MR(v) accounted for 34% of the decrease in total coronary resistance achieved by PCI. h-MR(v) of the target vessel after PCI was lower than that of the corresponding reference vessel despite a higher h-P(d) in the reference vessel (P<0.01). Post-PCI baseline MR(v) was correlated with baseline P(d) before PCI (P<0.01).
Conclusions:
PCI-induced restoration of P(d) resulted in a reduction of h-MR(v) in accordance with the pressure dependence of h-MR(v). The decrease in h-MR(v) to a level below that of the corresponding reference vessel in the immediate post-PCI period and a lowered baseline MR(v) suggest microvascular remodeling induced by long-term exposure to a low-pressure environment.
